Retinal vein occlusion (RVO) is a common cause of permanent visual loss and is the fifth cause of unilateral blindness in an Australian population-based study W. The most frequent and less severe type, branch retinal vein occlusion (BRVO) [2], is possibly driven by a mechanical factor because it generally occurs at an arteriovenous crossing [3]. The most rare and sight-threatening form, central retinal vein occlusion (CRVO) [2], remains of unknown pathophysiology [4,5].
Aging, arterial hypertension and glaucoma are the only well-established risk factors for RVO [6-8]. Despite a number of studies, thrombophilic risk factors have not been found to be associated with RVO, which suggests a very limited role of coagulation or anticoagulation factors in the pathophysiology of the disease [5,9]. In contrast, substantial data exist suggesting that blood hyperviscosity is an important risk factor. Several blood viscosity parameters have been shown to be increased in RVO patients compared with normal subjects, including a higher hematocrit, higher whole blood viscosity, reduced red cell deformability, and enhanced index of erythrocyte aggregation [7,10-14].
About 27% of patients with CRVO exhibit spontaneous in vitro growth of erythroid precursors in the absence of any detectable myeloproliferative disorder [15]. Red blood cells (RBCs) from patients with polycythemia vera have an abnormal CD239 (Lu/BCAM) phosphorylation, which is responsible for abnormal interactions with endothelial cells [16]. It was previously demonstrated that abnormal erythrocyte adhesion correlated with retinopathy in diabetes mellitus [17] and with vascular occlusion in sickle cell anemia [18].
There is no disclosure in the art of the increase of RBC adhesion to endothelial cells in CRVO, nor the role of PS or PS receptor in the increased CRVO RBC adhesion, nor the use of agent that inhibits the binding of phosphatidylserine to phosphatidylserine receptor in methods for treatment of retinal vein occlusion.
However, there is a need to develop new drugs that will be suitable for treatment of retinal vein occlusion. In this way, it has been suggested that characterisation of new therapeutic targets against RBC adhesion to endothelial cells in RVO may be highly desirable.